Oxidative stress, mitochondrial dysfunction, and ferroptosis in the placenta of gestational diabetes mellitus

Gestational diabetes mellitus (GDM) has become a significant concern in the domain of women's health. The pathophysiology of GDM is complicated and not entirely understood. As a functional interface of the maternal and fetal metabolisms, it is evident that the placenta exerts an effect on the development of GDM. The placenta not only involves itself in insulin resistance via the production of hormones, but also serves as an organ abundant in mitochondria and exhibits intense metabolic activities, rendering it particularly vulnerable to the adverse effects of oxidative stress. In the high-glucose environment, excessive oxidative damage leads to mitochondrial dysfunction and further induces ferroptosis by facilitating lipid peroxidation. The objective of this review is to predominantly assess recent research, published within the last five years, that investigates the roles of placental oxidative stress, mitochondrial dysfunction, and ferroptosis as pathological mechanisms influencing the development of GDM. Understanding these pathological changes may help to better explore novel therapeutic strategies for GDM.